Elevated EPO in aplastic anemia emerges from reduced erythroid mass and diminished receptor-mediated clearance; chronic kidney disease is consistent with impaired EPO synthesis and marrow suppression; anemia of chronic disease arises from reduced progenitor differentiation without requiring primary EPO failure; and shortened RBC lifespan alone does not lower steady-state EPO in hemolysis. This evidence concerns the gene EPO and idiopathic aplastic anemia.